Inhibition of regulator of G protein signaling 10, aggravates rheumatoid arthritis progression by promoting NF-κB signaling pathway.

摘要: Rheumatoid arthritis (RA) is the most common inflammatory arthropathy, with evidence pointing to an immune-mediated etiology that propagates chronic inflammation. Although targeted immune therapeutics and aggressive treatment strategies have substantially improved, a complete understanding of associated pathological mechanisms disease remains elusive. This study aimed at investigating whether regulator G protein signaling 10 (RGS10) could affect rheumatoid pathology by regulating response. A DBA/J1 mouse model RA was established evaluated for severity. RGS10 expression inhibited adeno-associated virus in vivo. Moreover, small interfering RNA used downregulate raw 264.7 cells vitro. Results showed inhibition augmented severity, attenuated increase factors. Furthermore, activated NF-κB pathways were detected following inhibition. These results revealed directly aggravated process activating pathway. Therefore, promising novel therapeutic target potential clinical impact.